When CDK4/6i meets GPX4i: Stop dividing to die iron hard

Deguang Liang; Xuejun Jiang

doi:10.1016/j.chembiol.2024.01.006

When CDK4/6i meets GPX4i: Stop dividing to die iron hard

Cell Chem Biol. 2024 Feb 15;31(2):187-189. doi: 10.1016/j.chembiol.2024.01.006.

Authors

Deguang Liang¹, Xuejun Jiang²

Affiliations

¹ Chinese Institutes for Medical Research, Beijing, China; Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Electronic address: liangd1@mskcc.org.
² Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA. Electronic address: jiangx@mskcc.org.

PMID: 38364774
DOI: 10.1016/j.chembiol.2024.01.006

Abstract

In this issue of Cell Chemical Biology, Rodencal et al.¹ report that cell-cycle arrest by p53 stabilizers or CDK4/6 inhibitors (CDK4/6i) can lead to phospholipid remodeling and hence sensitize cancer cells to GPX4 inhibitor (GPX4i)-triggered ferroptosis. This study suggests a novel cancer therapeutic strategy combining CDK4/6i with GPX4i.

MeSH terms

Ferroptosis*
Iron*
Phospholipids
Protein Kinase Inhibitors

Substances

Iron
Phospholipids
Protein Kinase Inhibitors